Author(s): FRANÇA, C., MUSTO, A., DO AMARAL, J., DE ABREU, D., SILVEIRA, A.L., BACHI, A., CARVALHO, R., Institution: SANTO AMARO UNIVERSITY, Country: BRAZIL, Abstract-ID: 171

INTRODUCTION:
Obesity is a multifactorial condition characterized by chronic low-grade inflammation resulting from the interaction between adipose tissue derived adipokines and inflammatory cytokines. White adipose tissue functions as an endocrine organ, playing a central role in the inflammatory profile observed in obesity. High-intensity interval training (HIIT) is known to reduce systemic inflammation; however, the physiological mechanisms by which exercise reorganizes adipokine-cytokine interactions remain poorly understood. This study aimed to investigate exercise-induced physiological adaptations in circulating adipokines, pro- and anti-inflammatory cytokines, and chemokines following HIIT in individuals with obesity.
METHODS:
One hundred and nine sedentary adults with obesity (BMI 30-40 kg/m2; 18-60 years; both sexes) were randomized to a non-exercising control group or an eight-week HIIT programme with three weekly sessions. Blood samples were collected at baseline (T0) and after 8 weeks (T1). Serum levels of adipokines (adiponectin, leptin, resistin, adipsin, RBP4), chemokines (MCP-1, IP-10), and inflammatory mediators (IL-1beta, IL-6, IL-8, IL-10, TNF-alpha, IFN-gamma) were measured using a multiplex assay. Comparisons were performed using the Wilcoxon and Kruskal-Wallis tests. Interaction analysis was used to identify exercise-induced physiological remodelling.
RESULTS:
After eight weeks of HIIT, triglycerides were reduced (p=0.009), with no changes in total cholesterol (p=0.309), LDL-C (p=0.666), HDL-C (p=0.088), non-HDL-C (p=0.351), or glucose (p=0.280). Between groups, differences were observed in total cholesterol (p=0.005), LDL-C (p=0.031), and non-HDL-C (p=0.017), with no differences in triglycerides (p=0.190), HDL-C (p=0.680), or glucose (p=0.153). HIIT reduced adiponectin (p=0.004), resistin (p=0.028), adipsin (p=0.020), IL-1beta (p=0.014), IL-10 (p=0.018), IFN-gamma (p=0.012), and IP-10 (p=0.023), while IL-6 (p=0.025) and IL-8 (p=0.025) increased. No changes were observed in leptin (p=0.413), TNF-alpha (p=0.219), or MCP-1 (p=0.255). Between groups, differences were found in leptin (p=0.039), IL-1beta (p=0.021), IL-10 (p=0.010), TNF-alpha (p=0.013), and IP-10 (p=0.007). Network analysis revealed that baseline and control profiles were characterized by pro-inflammatory mediators, particularly RBP4, IP-10, and TNF-alpha. In contrast, HIIT promoted the reorganization of the inflammatory profile, with IL-10 emerging as a central regulatory mediator and reduced adiponectin connectivity.
CONCLUSION:
HIIT induces physiological remodelling of the adipokine-cytokine network in obesity, promoting cardiometabolic benefits and reorganizing inflammatory control mechanisms. These findings support HIIT as an effective strategy for providing beneficial inflammatory adaptations in individuals with obesity, highlighting its potential role in modulating immune-metabolic integration and reducing the obesity-related inflammatory burden.